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Fenugreek in Management of Female-Specific Health Conditions
Published in Dilip Ghosh, Prasad Thakurdesai, Fenugreek, 2022
For regulatory purposes, a chemical’s mutagenicity potential has mainly been evaluated using in vitro assays, such as the Bacterial Reverse Mutation Test, AMES test (Mortelmans and Zeiger 2000). Mutagens are agents that can cause heritable changes in DNA, and their capacity to cause mutations is defined as mutagenicity (Cvetković, Takić Miladinov, and Stojanović 2018). As all information for the proper development, functioning, and reproduction of organisms is coded in DNA, mutations can result in harmful effects and play a role in genetic disorders (Verheyen 2017), especially for food-related products (Mandal et al. 2018; Weisburger 1999). The structural chromosomal abnormalities such as chromosomal aberration (a missing, extra, or irregular portion of chromosomal DNA) result from breakage and incorrect rejoining of chromosomal segments and result in many genetic diseases disorders such as cancer (Nguyen 2020). The standardized fenugreek seed extracts with markers such as furostenol saponins, glycosides, or low molecular galactomannans such as FENU-FG, SFSE-G, and LMWGAL-TF, were found safe and devoid of mutagenicity (OECD Test No. 471) and genotoxicity (Mammalian Chromosomal Aberration, OECD Test No. 473) potential during these studies (Deshpande, Mohan, and Thakurdesai 2016a; Deshpande, Mohan, Ingavale et al. 2017).
Introduction to Genomics
Published in Altuna Akalin, Computational Genomics with R, 2020
Mutations in the genome occur due to multiple reasons. First, DNA replication is not an error-free process. Before a cell division, the DNA is replicated with 1 mistake per 10^8 to 10^10 base-pairs. Second, mutagens such as UV light can induce mutations on the genome. The third factor that contributes to mutation is imperfect DNA repair. Every day, any human cell suffers multiple instances of DNA damage. DNA repair enzymes are there to cope with this damage but they are also not error-free, depending on which DNA repair mechanism is used (there are multiple), mistakes will be made at varying rates.
The Fight Against Cancer
Published in Nathan Keighley, Miraculous Medicines and the Chemistry of Drug Design, 2020
Cancer can be caused by environmental influences, such as carcinogenic chemicals, example in cigarette smoke or in certain foods, which induce gene mutations or interfere with normal cell differentiation and division. Genetic mutation in genes that are responsible for controlling cell division can result in uncontrolled multiplication of cells to produce a tumour. In this way, mutagenic chemicals can result in carcinogenesis; the development of cancer.
Radiosensitivity of seedling traits to varying gamma doses, optimum dose determination and variation in determined doses due to different time of sowings after irradiation and methods of irradiation in faba bean genotypes
Published in International Journal of Radiation Biology, 2023
Rajdeep Guha Mallick, Subhradeep Pramanik, Manas Kumar Pandit, Akhilesh Kumar Gupta, Subhrajit Roy, Sanjay Jambhulkar, Ashutosh Sarker, Rajib Nath, Somnath Bhattacharyya
To initiate an induced mutagenesis programme the first step is to select a suitable mutagen. A long-held idea, which probably has been influencing the choice of mutagen (chemical vs. physical) is that the chemical mutagens more favorably induce point mutations, whereas physical mutagens encourage gross lesions, such as chromosomal aberration and rearrangement. The chemical mutagens are said to be highly toxic. On the other hand, the side effects on the health caused by physical mutagens are considerably less. The choice of mutagen completely depends on its availability, allied expenditures and existing infrastructures. Gamma rays are quite easy in application; it penetrates easily due to their non-particulate nature and causes higher mutation frequency. In this experiment, gamma rays have been used for seed irradiation.
Acrylonitrile’s genotoxicity profile: mutagenicity in search of an underlying molecular mechanism
Published in Critical Reviews in Toxicology, 2023
Richard J. Albertini, Christopher R. Kirman, Dale E. Strother
The difference between direct and indirect mutagenicity is that, while direct effects imply specific interactions with the genetic material, i.e. ACN → DNA interaction not requiring intermediary cellular processes, the mechanism by which ACN indirectly affects the DNA is multi-step (Figure 3; Albertini and Kaden 2020). A direct reaction with the DNA is the concept that forms the basis of the “one hit” non-threshold model of chemical carcinogenesis for mutagenic carcinogens whereby a single interaction with the DNA minimally raises the probability of cancer, even when undetectable by observation. This concept has been challenged (Heflich et al. 2020) but its validity is not the focus of this review. In contrast to direct genotoxicity, an exogenous chemical or its metabolite may indirectly damage the genetic material via a series of interactions with various cellular components leading to alterations of function and/or production of endogenous mutagens and/or reduction of defenses, i.e. exogenous chemical → cellular processes → production of endogenous mutagens → reduction of defenses → ± altered cellular functions. The mechanisms by which exogenous mutagens indirectly damage DNA do not fit the direct model in that there will be a dose effect for chemical interactions with cellular processes that is likely amplified when a series of processes are required before mutations are produced.
Investigation of oxidative damage, antioxidant balance, DNA repair genes, and apoptosis due to radiofrequency-induced adaptive response in mice
Published in Electromagnetic Biology and Medicine, 2022
Yusuf Kucukbagriacik, Mohammadreza Dastouri, Elcin Ozgur-Buyukatalay, Ozen Akarca Dizakar, Korkut Yegin
Bleomycin is an antineoplastic chemotherapy agent causing chromosomal aberrations, so it has been used in therapeutic chemotherapy to treat different cancers (Bolzán and Bianchi 2018; Schlade-Bartusiak et al. 2002; Zong et al. 2015). The exposure of cells or animals to low dose non-ionizing radiation, ionizing radiation, or chemical agent, to subsequently become resistant to toxic damage caused by exposure to a challenge dose (CD) of ionizing radiation or chemical agent is called adaptive response (Vijayalaxmi and Scarfi 2014. The adaptive response phenomenon was first demonstrated in Escherichia coli in 1977 (Samson and Cairns 1977). The non-toxic dose of mutagens is usually referred to as adaptation dose (AD) and the toxic dose of mutagens as a CD. The challenge dose of mutagens causes significant damage to cells and organisms. Studies exhibited that this damage was reduced with the adaptive response effect when RF was used before the CD (Falone et al. 2018; Zong et al. 2015). For example, the latest experiments have showed that the exposure to RF before CD of chemical agents (bleomycin, etc.) (Sannino et al. 2011; Zeni et al. 2012; Zong et al. 2015) or ionizing radiation (Cao et al. 2011; Jiang et al. 2013) in in-vivo and in-vitro conditions dramatically reduced the levels of DNA damage when compared to CD only.